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INVITED REVIEW

Aggressive periodontitis: A review

Vaibhavi Joshipura, Umesh Yadalam, Bhavya Brahmavar1
Departments of Periodontics, Sri Rajiv Gandhi College of Dental Sciences and Hospital, Cholanagar, Bangalore, 1Periodontics, Mathikeri Sampige
Ramaiah College of Dental Sciences and Hospital, Affiliated to Rajiv Gandhi Health University, Bengaluru, Karnataka, India

ABSTRACT
The purpose of this review is to highlight the current etiological and therapeutic concepts of aggressive Access this article online
periodontitis which is rapidly progressing and aggressive in nature. It leads to destruction of periodontal Website: www.jicdro.org
tissues and loss of teeth. We need advanced diagnostic techniques to learn about current disease DOI: 10.4103/2231-0754.153489
activity and rate of progression. We also require strategies to keep the disease under control with proper Quick Response Code:
maintenance regime and prevent tooth loss, because it can result into complicated prosthetic rehabilitation
in a very young patient. The evidence suggests that aggressive periodontitis is influenced by microbiological,
genetic, and host factors. This paper reviews clinical, microbiological, immunological, and genetic aspects
of pathogenesis of aggressive periodontitis, as well as diagnostic criteria of the disease and appropriate
nonsurgical and surgical treatment options.

Key words: Aggressive, genetic, host factors, microbiologic, periodontitis

INTRODUCTION
Aggressive periodontitis generally affects systemically healthy
individuals less than 30 years of age, though patients may
be older. Aggressive periodontitis is distinguished from
chronic periodontitis by the age of onset, the rapid rate
of destruction, composition of the subgingival microflora,
alteration in the host immune response, familial aggregation
of diseased individuals, and a strong racial influence.
HISTORY
Black in the year 1886, [1] used the terms phagedenic
pericementitis and chronic suppurative pericementitis to
describe patients who suffered from a rapid destruction of
alveolar bone. Gottlieb in the year 1923 described an unusual
form of periodontal disease that involved some or all of the
permanent incisors and first molars of young individuals.
Based on histological observations on extracted teeth from
affected sites, he believed that the disease was due to
defective deposition of cementum or cementopathia. Gottlieb
in the year 1928 applied the principles of classical pathology,
which stated that all human nonneoplastic diseases could
be classified as either inflammatory or noninflammatory
Address for correspondence:
Dr. Vaibhavi Joshipura, Department of Periodontics, Sri Rajiv Gandhi
College of Dental Sciences and Hospital, Affiliated to Rajiv Gandhi Health
University, Cholanagar, R T Nagar post, Bangalore - 560 032, India.
E-mail: vaibhavi_joshipura@yahoo.co.in
and used the term diffuse atrophy of the alveolar bone[2] to
describe a condition in which adolescent patients did not
exhibit the intense gingival inflammation ordinarily seen in
other adult patients with periodontitis, he believed that the
disease was a noninflammatory or degenerative condition.
In the year 1942, Orban and Weinmann introduced the
term periodontosis to describe the periodontal destruction
in young individuals.[3] At the 1966 World Workshop in
Periodontics, it was concluded that there is no evidence for
the existence of noninflammatory degenerative periodontal
disease and the term periodontosis should be eliminated
from periodontal nomenclature. In the late 1970s and early
1980s, it was believed that the condition was an infection that
could be treated by therapy based on excellent plaque control
and the idea that the disease may be due to degeneration of
cementum, or any other components of the periodontium,
was laid to rest. As a reflection of this changing opinion
regarding the etiology of the disease in 1969 Butler[4] used the
term juvenile periodontitis andreplaced periodontosis and
in 1989 as early onset periodontitis[5] as the preferred term
for the condition. In the1999 classification system, the name
of the disease was changed to aggressive periodontitis,[6]
the reason being to eliminate nonvalidated age-dependent
designations.
CASE DEFINITION AND DIAGNOSTIC CRITERIA
In 1971, Baer defined aggressive periodontitis as a disease of
the periodontium occurring in an otherwise healthy adolescent,

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Joshipura, et al.: Aggressive periodontitis
which is characterized by a rapid loss of alveolar bone around
more than one tooth of the permanent dentition.[7]
Definition: Disease of the periodontium occurring in an
otherwise healthy adolescent, which is characterized by
rapid loss of alveolar bone about more than one tooth of
the permanent dentition. The amount of destruction is not
commensurate with the amount of local irritants.
A contemporary case definition of aggressive periodontitis
is presented by Albandar in 2014.[8]
Key diagnostic criteria of this disease include an:
• Early age of onset,
• Involvement of multiple teeth with a distinctive pattern of
clinical attachment loss and radiographic bone loss, and
• A relatively high rate of disease progression and the
absence of systemic diseases that compromise the host’s
response to infection.
• Although in some patients the disease may start before
puberty, in most patients the age of onset is during, or
somewhat after, the circumpubertal period. A typical
patient shows disease onset at an early age (i.e., before
25 years of age), although identification of the affected
patient usually occurs after disease commencement.
• Initially, the periodontal lesions show a distinctive pattern,
depicted radiographically as vertical bone loss at the
proximal surfaces of posterior teeth, and the bone loss
usually occurs bilaterally. In advanced cases of aggressive
periodontitis the periodontal lesions may be depicted
radiographically as a horizontal loss of bone. The primary
teeth may also be affected, although early exfoliation of
these teeth is not common.
• Aggressive periodontitis may be localized or generalized,
in localized aggressive periodontitis (LAP), tissue loss
usually starts at the permanent first molars and incisors,
and with increasing patient age the disease may progress
to involve the adjacent teeth. The generalized form
of aggressive periodontitis involves most or all of the
permanent teeth.
CLASSIFICATION
1. Localized aggressive periodontitis (LAP): Localized to first
molar/incisor interproximal attachment loss
2. Generalized aggressive periodontitis (GAP): Generalized
interproximal attachment loss affecting at least three
permanent teeth other than incisors and first molar.
EPIDEMIOLOGY
The prevalence of L AP varies considerably between
continents, and differences in race/ethnicity seem to be a
major contributing factor.
12 Journal of the International Clinical Dental Research Organization | January-June 2015 | Vol 7 | Issue 1
Estimates of the disease prevalence are 1-5% in the African
population and in groups of African descent, 2.6% in
African-Americans, 0.5-1.0% in Hispanics in North America,
0.3-2.0% in South America, and 0.2-1.0% in Asia.
Among Caucasians, the disease prevalence is 0.1% in northern
and in central Europe, 0.5% in southern Europe, and0.1-0.2%
in North America.
The prevalence of LAP is less than 1% and that of GAP is 0.13%.
Blacks are at higher risk than whites, males are at higher risk
of GAP than females. In Asia the prevalence rate of 1.2% for
LAP and 0.6% for GAP in Baghdad and Iran population, and
0.47% in Japanese population.[9]
CLINICAL FEATURES
LAP starts at circumpubertal age, involving interproximal
attachment loss of first molar, and or incisors, there will
be lack of inflammation with presence of deep periodontal
pocket and advanced bone loss. Amount of plaque is minimal
which is inconsistent with the amount of destruction,
and rarely mineralizes to form calculus, but the plaque is
highly pathogenic due to the presence elevated levels of
bacteria like Aggregatibacter actinomycetumcomitans (A.a) and
Porphyromonas gingivalis (P.g). Secondary clinical features like
distolabial migration of incisors with diastema formation,
mobility of the involved teeth, sensitivity of the denuded
root, deep dull radiating pain to the jaw, and periodontal
abscess lymph node enlargement may occur.[10]
GAP has generalized interproximal attachment loss affecting
at least three permanent teeth other than incisors and first
molar involving individuals under age 30 with destruction
appears to occur episodically. There will be presence of
minimal plaque which is inconsistent with destruction and
presence of bacteria like P.g, A.a, and Tannerella forsythia are
detected in plaque.[10]
Two kinds of gingival responses are seen in GAP patients. First
response is severe acutely inflamed tissue which is ulcerated
and red in color with spontaneous bleeding indicating
destructive stage and the other one with pink gingiva free
of inflammation, with some degree of stippling and deep
periodontal pockets are present representing quiescence
stage.[10]
HISTOPATHOLOGY
Histopathology of aggressive periodontitis is not well-
documented as compared to chronic periodontitis because of
less numbers of aggressive periodontitis patients, changing
the definition of disease entity, and variations in the timing
of the biopsies.
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Joshipura, et al.: Aggressive periodontitis
However, Stambolieva and Bourkova[11] found increase in
the numbers of acid phosphatase positive macrophages
(phagocytic macrophages) in aggressive periodontitis
patients. In the pretreatment biopsies of LAP, there was
predominant plasma cell inflammatory infiltration,[12] and
the root surfaces of individuals with aggressive periodontitis
were observed to beheavily covered by neutrophils.[13] A fully
developed lesion consists ofplasma cell dominated infiltration
in the connective tissue with neutrophils migrating through
the pocket lining epithelium and creating a layer between
the plaque and tissues.
MICROBIOLOGY
Use of advanced microbiological methods has improved
our knowledge regarding the composition of bacteria in
subgingival deposits which can cause different forms of
periodontitis. There are geographic and ethnic variations in
relation to periodontitis associated microorganisms.
Since long time A.a has been considered the primary
pathogen for aggressive periodontitis, especially in its
localized form. Six serotypes of A.a (a, b, c, d, e, and f) are
described based on the composition of O polysaccharide
of their lipopolysaccharide and there are phenotypically
nonserotypeable strains of A.a which lack expression
of serotype-specific polysaccharideantigen. [14] A highly
leukotoxic clonal type of A. A serotype b was first isolated, in
the early 1980s, from an 8-year-old male child with localized
aggressive periodontitis.[14] Prevalence of A.a in LAP varies
from 70 to 90%,[15,16] but there are studies which states there is
no association between A.a and the periodontal diseaserather
prevalence of levels of P.g, T.denticola, and P.intermedia are
significantly associated withaggressive periodontitis. In a
study done by Takeuchi for detection of microorganisms in
sub gingival flora of Japanese population using polymerase
chain reaction (PCR) it was found that the prevalence of
A.a was less in patients with LAP whereas elevated levels
of P.g, Tannerella forsythia, T.denticola, P.intermedia, and
Campylobacterrectus was detected.[17] Albander found elevated
levels of IgG and IgA to P.g and A.a and IgA to P.intermedia in
subjects with GAP than LAP and no difference was found at the
antibody levels of C.rectus, E. corridens, F.nucleatum.[18] Filifactor
alocis is gram positive anaerobic rod which has the potential
of being periodontal pathogen and the levels of these bacteria
is elevated in aggressive periodontitis patients.[19] Treponema
lecithinolyticumand Treponema socranskii are elevated in GAP.[20]
Sulfate reducing bacteria, Desulfomicrobium orale, has been
suggested to be involved in various categories of periodontal
destruction, possibly synergistically with the red complex
periodontal pathogens.[21] Yamabe suggested Archaea a
methanogenic organism, especially Methanobrevibacter oralisas
putative periodontal pathogen for aggressive periodontitis.[14]
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Herpes viruses, especially Epstein-Barr virus (EBV) and
human cytomegalovirus, have been suggested to play a role
in the onset of aggressive periodontitis by interacting with
periodontitis-associated bacteria, such as A.a, P.g, T. forsythia,
C. rectus, Dialister pneumosintes.[22]
ROLE OF GENETICS IN AGGRESSIVE PERIODONTITIS
In periodontitis, the host-activated inflammatory and
immunological cascades responding to predominantly
gram-negative microorganisms that result in the destruction
of connective tissue and bone are under genetic control.
Genetic and environmental factors play a crucial role in
the development of aggressive periodontitis. Here are few
gene polymorphism and their associations with aggressive
periodontitis.
A strong association was found between interleukin (IL)-1a
(889)[23] and IL-1a 3954allele 2 polymorphism[24] and aggressive
periodontitis. IL-1 gene cluster was not associated with AP
according to Fiebig in caucasians.[25] IL-4-590 T/T, IL-4-34 T/T
genotype are associated with AP.[26] IL-6-174G allele increased
the risk of AP and IL-6-572 C/G polymorphism is associated
with pathogenesis.[27] Nibali found link between IL-6-1363,-
1480 polymorphism and LAP susceptability.[28].IL-10 promoter
polymorphisms at positions -1082 G-A,-819C-T, and -590C-A
showed that haplotype ATA is a putative risk indicator for
GAP.[29] FPR348 T-C gene polymorphism showed association
with AP in African American subjects.[30] Fc gamma RIIIb-NA2
allele and Fc gamma RIIIb-NA2/NA2 genotype and composite
genotype FcaRIIIb-NA2/NA2 and FCgammaRIIIa-H/H131 may
be associated with GAP.[31] FCgamma polymorphisms can
lead to modulation of neutrophil superoxide production
and predispose to AP.[32] VDR, FcaRIIIb composite genotype
may be associated with susceptibility to generalized early
onset periodontitis.[33] TLR-4 399 Ile polymorphism showed a
protective effect against AP.[34] TNFA gene polymorphism (1031,
863,857, 308, and 238) was not associated with aggressive
periodontitis.[35] HLA-DR4, HLA-A9, B-15 are found in high
frequency in rapidly progressive periodontitis patients[36,37]
and HLA-DQB1 plays a crucial role in pathogenesis of AP.[38]
Miscellaneous genes associated with aggressive periodontitis
are AGT-angiotensinogen CTSC-cathepsin C, E-selectin in
Iranian population, FPR-formyl peptide receptor in Asian
population, NADPH-NADPH oxidase, PAII-plasminogen
activator inhibitor 1, and S100A8-calprotectin in Asians,
TIMP2-tissue inhibitor of matrix metalloproteinase 2 in
Asians, and t-PA-tissue plasminogen activator in Caucasian.
HOST RESPONSE
Aggressive periodontitis should be present in a healthy
individual; multiple systemic conditions may be associated
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Joshipura, et al.: Aggressive periodontitis
with attachment loss which needs to be ruled out before
giving the diagnosis as aggressive periodontitis because
in conditions like leukocyte adhesion deficiency syndrome
and Papillon-Lefevre syndrome the oral picture resembles
aggressive periodontitis. Polymorphonuclear neutrophils
(PMNs) play an important role in host immune response,
qualitative and quantitative deficiency in PMNs can lead to
increased periodontal destruction, and this does not mean
aggressive periodontitis is caused by dysfunctional PMNs.
Although host factors can also play an enormous role in the
progression of disease, PMN dysfunction does not appear
to be a cause for aggressive periodontitis in nonsyndromic
individuals.[39]
TREATMENT
The overall treatment concepts and goals in patients with
aggressive periodontitis are not markedly different from
those in patients with chronic periodontitis. Therefore, the
different treatment phases (systemic, initial, reevaluation,
surgical, maintenance, and restorative) are similar for both
types of periodontitis. However, the considerable amount of
bone loss relative to the young age of the patient and the high
rate of bone loss warrants a well-thought-through treatment
plan and an often more aggressive treatment approach, in
order to halt further periodontal destruction and regains as
much periodontal attachment as possible.[40]
NONSURGICAL PERIODONTAL THERAPY
Scaling and root planing
Scaling and root planing in patients with LAP improves the
clinical parameters, but with the limited data present it is
unclear to know the predictability and long-term stability
of scaling and root planing (SRP) in LAP. The effect of SRP
is well-documented in patients with GAP. Patients with GAP
respond well to SRP in short term (6 months), after 6 months,
relapse, and disease progression is reported despite frequent
recall visits and oral hygiene reinforcements.[40]
Systemic antibiotics
Treating patients with aggressive periodontitis is challenging.
The disease responds less predictably to conventional
mechanical periodontal therapy, hence scientists have been
exploring adjunctive treatment to improve the outcome,
predictability of the conventional mechanical therapy. In view
of the specific microbial nature of aggressive periodontal
disease, the use of systemic antibiotics can play an important
role in the treatment of these diseases.
Systemic antibiotics like tetracycline, metronidazole,
combination of metronidazole and amoxicillin, clindamycin,
and azithromycin are also used as adjunct in the treatment
of aggressive periodontitis. Slots and Rosling, Kornman and
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Robertson, Asikainen, Palmer, and Tinoco, did studieson
SRP in combination withantibiotics in LAP patients. Sigush,
Guerrera, Hass, Yek, Mestnik, and Aimetti did studies on SRP
in combination with antibiotics in GAP patients. The studies
concluded that using antibiotics as an adjunct to SRP is
beneficial when compared to SRP alone in treating aggressive
periodontitis. Combination of amoxicillin and metronidazole
with SRP is effective in treating GAP.[40]
Local antimicrobials
Agents like 1% chlorhexidine gel, 40% tetracycline gel,
tetracycline fibers, and chlorhexidine chip have been used
as local antimicrobials in the treatment of LAP and GAP.
Unsal, Purucker, Kaner, and Sakellari have done studies on
treating aggressive periodontitis using local antimicrobials.
The studies concluded that the adjunct effect of local
antimicrobial is not clear and do not seem to improve on
the adjunct effect of systemic antibiotics. Therefore, it seems
reasonable that the decision to use this type of treatment
modality should be made on an individual basis rather than
be evidence-based.[40]
SURGICAL THERAPY
Access surgery
Modified Widman flap surgery alone or in combination with
tetracycline is effective in reducing the pocket depths and
pathological microbial load. Modified Widman flap with
systemic administration of amoxicillin and metronidazole
combination is also beneficial in treating aggressive
periodontitis. Christersson, Lindhe and Liljenberg, Mandell
and Socransky, and Buchman have done extensive research
on access surgery alone or in combination with antibiotics in
treating aggressive periodontitis and concluded that access
surgery in combination with systemic antibiotics was effective
than access surgery alone.[40]
Teeth used as abutments for fixed constructions in aggressive
periodontitis patients are more prone for extractions during
follow-up period of 10 years (Yi et al., 1995 and Lulic et al.,
2007). Pretzel indicated double rate of tooth loss used as
abutments in fixed constructions over 10 years than teeth
that are not used as abutments. The reason might be because
of decreased accessibility for cleaning leading to risk for
reinfection and progression of disease.[41]
IMPLANTS
According to short-term studies, the survival rate of
implants in GAP patients is around 97.4-100%; whereas
that of long-term studies, survival ranges from 83.3 to 96%.
Therefore, implant treatment in patients with GAP is not
contraindicated, provided that adequate infection control
and an individualized maintenance program is assured.[42]
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AGGRESSIVE PERIODONTITIS IN INDIAN
POPULATION
In a cross-sectional survey done to know the prevalence of
aggressive periodontitis in Moradabad population with their
systemic manifestations, it was concluded that the frequency
of systemic manifestations such as fatigue, weight loss,
and loss of appetite was significantly greater in aggressive
periodontitis and a significant correlation between anxiety/
depression and aggressive periodontitis was observed.[43]
In a study done by Rahul et al., neutrophil functions like
chemotaxis, phagocytosis, and microbicidal activity, are
deficient in LAP patients. These abnormal neutrophil
functions may predispose to increased susceptibility for
LAP.[44]
The incidence of A.a along with P.g and T. forsythia was high
in aggressive periodontitis patients in subgingival plaque in
south Indian population.[45] Viruses like herpes simplex virus
(HSV)-1 and EBV were found to be significantly associated
with destructive periodontal disease, including chronic
and aggressive periodontitis. Further, HSV-1 was found to
be associated with severity and progression of destructive
periodontal disease.[46]
FcγRIIIa V/V genotype and/or V allele, as well as the FcγRIIIb
NA2/NA2 and/or NA2 allele, along with the FcγRIIa-R allele,
may be risk factors for generalized aggressive periodontitits
(GAgP) in the population of South India.[47] In a study done
by Shete et al., there was no gene polymorphism found
in patients with aggressive periodontitis.[48] In Malayalam
speaking Dravidian population, IL-4 + 33C/T loci appears
to be an important risk factor for periodontal disease
with a leaning towards aggressive periodontitis.[49] The
association between IL-17F at 7383A/G and 7488A/G loci
with either chronic or an aggressive periodontitis could not
be ascertained.[49] In a study to know the clinical and genetic
aspects of GAP in families of Tumkur district in Karnataka, it
was concluded that the disorder may not be segregating as
an autosomal recessive trait and could have been misled by
consanguinity in the family and it could be a multifactorial
trait, or still segregating as an autosomal recessive trait, but
the region of homozygosity could be small.[50]
Systemic administration of doxycycline with full mouth SRP
resulted in a better improvement of periodontal parameters
and elimination/suppression of putative periodontal
pathogens such as A.a, P.g, and T. forsythia, than amoxicillin
plus metronidazole in patients with LAP.[51]
CONCLUSION
Aggressive periodontitis affects smaller percentage of
population, which is influenced by specific bacterial etiology,
Journal of the International Clinical Dental Research Organization | January-June 2015 | Vol 7 | Issue 1
host response, and genetic factors. As the disease is rapidly
progressing and aggressive in nature, these patients require
early diagnosis and treatment to prevent further progression
of the disease and tissue damage.
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Cite this article as: Joshipura V, Yadalam U, Brahmavar B. Aggressive
periodontitis: A review. J Int Clin Dent Res Organ 2015;7:11-7.
Source of Support: Nil. Conflict of Interest: None declared.
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Joshipura, et al.: Aggressive periodontitis

About the author

Dr. Vaibhavi Joshipura has done her M.D.S. in Periodontics from Government Dental College and Hospital, Ahmedabad,
Gujarat, in 1995, and currently pursuing her PhD from Gujarat University. She is Post Graduate guide with over 19 years of
teaching experience and has been working as specialist consultant in Periodontics with various hospitals and dental clinics
in Bengaluru since 1996. At present she is Principal and professor of periodontology at Sri Rajiv Gandhi College of dental
sciences and hospital, Bengaluru. She has lectured at various national conferences and CDE programs. She has several
national and international publications to her credit. She has received research grant from Siddhartha University for her
research at Indian Institute of Science Bengaluru, on genetic aspects of aggressive periodontitis in Tumkur population. She
is a reviewer for various national and international journals like Journal of Indian society of Periodontology, International
Journal of Health & Allied Sciences –JSS University, Journal of Annual research and review in Biology-Science domain
international, and Journal of international clinical dental research organization. She is on editorial board of IDES journal
of research and practice of dental science, and chief editor of Dental era-Journal of dentistry.

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